Podcasts about abdominal aortic aneurysm

Today's episode is the second of our two part series on ruptured AAA repairs. We discuss the case of a 72 year old man with a ruptured abdominal aortic aneurysm that is contained, and who is scheduled for an urgent endovascular repair within the interventional radiology suite with special guest, Dr Lahiru Amaratunge.Apologies for the audio quality in this episode - even though it sounds like we recorded on a submarine, we can assure you we were sitting in our study the entire time. Resources for today's episode:BJAED: Anaesthesia for endovascular repair of ruptured abdominal aortic aneurysmsby K. Berry et al.LITFL: AAA by C. NicksonLancet: Endovascular versus open repair of abdominal aortic aneurysm in 15-years' follow-up of the UK endovascular aneurysm repair trial 1 (EVAR trial 1): a randomised controlled trial by Patel, R. et al.Annals of Surgery: Endovascular Repair of Abdominal Aortic Aneurysm in Patients Physically Ineligible for Open Repair: Very Long-term Follow-up in the EVAR-2 Randomized Controlled Trial by Sweeting, M. et al.Feel free to email us at deepbreathspod@gmail.com if you have any questions, comments or suggestions. We love hearing from you! And don't forget to claim CPD for listening if you are a consultant or fellow. Log us as a learning session which you can find within the knowledge and skills division, and as evidence upload a screenshot of the podcast episode. Thanks for listening, and happy studying!

Today - in part 1 of our 2 part series - we talk through the case of an 82 year old man with a ruptured abdominal aortic aneurysm who is scheduled for urgent open repair with special guest, Dr Lahiru Amaratunge.Resources for today's episode:BJAED: Anaesthesia for endovascular repair of ruptured abdominal aortic aneurysms by K. Berry et al.LITFL: AAA by C. NicksonLancet: Endovascular versus open repair of abdominal aortic aneurysm in 15-years' follow-up of the UK endovascular aneurysm repair trial 1 (EVAR trial 1): a randomised controlled trial by Patel, R. et al.Annals of Surgery: Endovascular Repair of Abdominal Aortic Aneurysm in Patients Physically Ineligible for Open Repair: Very Long-term Follow-up in the EVAR-2 Randomized Controlled Trial by Sweeting, M. et al.Feel free to email us at deepbreathspod@gmail.com if you have any questions, comments or suggestions. We love hearing from you! And don't forget to claim CPD for listening if you are a consultant or fellow. Log us as a learning session which you can find within the knowledge and skills division, and as evidence upload a screenshot of the podcast episode. Thanks for listening, and happy studying!

Commentary by Dr. Candice Silversides

With Omar Hahad & Andreas Daiber, University Medical Center of the Johannes Gutenberg University Mainz, Mainz - Germany Link to paper Link to editorial

Welcome to the AAA-Team's special episode of Join the Docs, and today, we're exploring the explosive world of abdominal aortic aneurysms (AAA) starring your favourite dynamic duo with their trusty sidekick Slim the skeleton! It's no joke - this condition is a big deal, so join Doctor Nigel Guest and Professor Jonathan Sackier and buckle up for a rib-tickling ride through the twists and turns of AAA.Your aorta, the main blood vessel supplying your gut, kidneys assorted organs, pelvis, and legs, suddenly decides to blow up like a balloon. That's what we call an abdominal aortic aneurysm. But set your funny bones aside, because if that balloon bursts, it's no party — it can be life threatening! AAA can be triggered by a variety of genetics and lifestyle choices, with smoking, high blood pressure, and sky high cholesterol levels being the usual suspects.Now, the symptoms of AAA are sneaky little devils. So what should you look out for? Chronic back pain and discomfort “downstairs” are two tell-tale signs. If not addressed, AAA can even cause sudden death! But fear not, The Docs are here to make sure you're armed and ready to tackle it head-on.Prevention and early detection are our bread and butter (well…easy on the butter). What measures can be taken, especially even for over 55s accustomed to smoking a pack of 20 cigarettes daily, or individuals with a family history of health issues, even if they seem perfectly healthy? The Docs discuss screening techniques like ultrasound and CT scans to proactively catch an abdominal aortic aneurysms (AAA) before it catches you.For the itty-bitty, less immediately serious aneurysms, it's a good idea to keep them in your peripheral vision, with regular screening. But if they start getting too big for their boots, it's time to ‘go all in' and have a surgeon visit your AAA. Whether it's performing surgery to address abdominal issues or inserting a stent to protect your arteries, rest assured, we've got the right tools to fix you up good as new.It's not all about what we can do in the operating room. Lifestyle changes are the real superheroes here. Quitting smoking, reducing your blood pressure, and keeping cholesterol levels in check are the ways to go. Hard to stomach, but worth the change.So, remember, knowledge is power! Stay on top of your health, get regular check-ups, and don't be afraid to make some changes along the way. With a bit of know-how and the right care, we'll beat AAA together and keep you laughing all the way to good health!—--DISCLAIMER: The views and opinions expressed on Join the Docs are those of Dr. Nigel Guest, Jonathan Sackier and other people on our show. Be aware that Join the Docs is not intended to be medical advice, it is for information and entertainment purposes only - please, always take any health concerns to your doctor or other healthcare provider. We respect the privacy of patients and never identify individuals unless they have consented. We may change details, dates, place names and so on to protect privacy. Listening to Join the Docs, interacting on our social media, emailing or writing to us does not establish a doctor patient relationship. To Contact Us: For a deeper dive on this episode's issue, merchandise and exclusive content, head to www.jointhedocs.comFollow us on youtube.com/JoinTheDocs Follow us on instgram.com/JoinTheDocsFollow us on tiktok.com/JoinTheDocsFollow us on: facebok.com/JoinTheDocs Follow us on: x.com/JoinTheDocs

No one cares about you, more than YOU. It's time to put your health first. In this episode, we share some tips to take charge of your own health and preventative care you can do to get ahead of things that may arise. Special thank you to Amber Nease for sharing information about LifeLine Screening, which we discuss in this episode. LifeLine Screening has screening packages that check your risk for Kidney Disease, Osteoporosis, HsC Reactive Protein, A1c Screening, Thyroid Hormone, Prostate & Testosterone Screening, Liver Panel, Atrial Fibrillation, Arterial Disease, Cartoid Artery Scan, Abdominal Aortic Aneurysm test and more. The link to learn more and book a screening is: https://www.lifelinescreening.com/screening-services?sourcecd=WABF005. Stay tuned for our upcoming workshops at: https://www.thetimetogrow.com/. The importance of self-care (00:00:00) Scott and Nancy introduce the episode's topic, emphasizing the need for self-care and preventative health measures for entrepreneurs and business owners. Inspiration from Marie Forleo (00:00:57) Nancy shares how an episode by Marie Forleo inspired the discussion, highlighting the importance of health and simple measures to prolong life. Personal health experiences (00:01:57) Scott and Nancy share personal health experiences and the significance of self-care in preventing health issues. Diagnosis and lifestyle changes (00:04:52) Nancy discusses her diagnosis of hypothyroidism and Hashimoto's, emphasizing the importance of dietary changes and medical treatment. Unexpected health discovery (00:07:31) Nancy recounts the discovery of kidney cancer and the importance of being proactive in seeking medical attention and advocating for one's health. Lifeline screening program (00:10:44) Nancy introduces the Lifeline screening program, emphasizing the value of preventative care and early detection for chronic illnesses. Healthy habits and dietary changes (00:13:35) Scott discusses his dietary habits, including the use of organic shakes and supplements, and the importance of maintaining a healthy diet. Optimism and sugar consumption (00:17:07) Nancy highlights the benefits of optimism in prolonging life and emphasizes the importance of cutting back on sugar consumption for better health. Get at least eight hours of sleep (00:19:11) Importance of sufficient sleep for adults and children, its impact on overall health. Work out three days a week (00:19:28) Benefits of regular exercise in preventing diseases, strengthening bones and organs, and improving metabolism. Eat healthy (00:20:17) Emphasizing the significance of making healthy food choices for overall well-being and disease prevention. Genetics and lifestyle choices (00:21:12) Discussion on the influence of genetics and lifestyle choices on physical well-being, including a surprising statistic about genetic predisposition. Changing the genetic makeup (00:22:10) How lifestyle choices can change the chemical makeup of DNA and be passed down through generations. Resources for preventative health screenings (00:23:13) Recommendation for a health screening service and the importance of proactive health measures. Proactive measures for preventing health issues (00:25:02) Personal experiences and proactive measures for preventing health issues, including the importance of regular health screenings and sun protection. Importance of self-care for overall well-being (00:26:09) Emphasizing the impact of self-care on overall well-being and the recommendation for proactive health measures. These timestamps cover the topics discussed in the given podcast episode transcription segment.

No one cares about you more than YOU. It's time to put your health first. In this episode, we share some tips to take charge of your own health and preventative care you can do to get ahead of things that may arise.  Special thank you to Amber Nease for sharing information about LifeLine Screening, which we discuss in this episode. LifeLine Screening has screening packages that check your risk for Kidney Disease, Osteoporosis, HsC Reactive Protein, A1c Screening, Thyroid Hormone, Prostate & Testosterone Screening, Liver Panel, Atrial Fibrillation, Arterial Disease, Cartoid Artery Scan, Abdominal Aortic Aneurysm test and more. The link to learn more and book a screening is: https://www.lifelinescreening.com/screening-services?sourcecd=WABF005"

Commentary by Dr. Valentin Fuster

Host Mike Moore interviews Co-Founder & Chief Medical Officer, Dr. Randy Moore of ViTAA Medical. ViTAA's AI-backed SaMD offers precision, personalized medicine to non-invasively map the strength and weakness of abdominal aortic aneurysms (AAA). ViTAA's RAW™ (Regional Areas of Weakness) Map technology can analyze the deformation of the aorta wall using images captured throughout the cardiac cycle. Then, by incorporating critical simulation data on blood flow and the location and size of clots (ILT or intraluminal thrombus) within the aneurysm, ViTAA's algorithms compute and generate detailed vulnerability maps of the abdominal aortic aneurysm. The technology is available as part of the ViTAA Registry which has been launched in 8 North American sites. Further access to the technology will also be possible through ViTAA's Research Use Only Program, which was initiated in late 2022. Resources & Links Mike Moore https://www.linkedin.com/in/michaeljeffreymoore/ https://www.linkedin.com/company/thebleedingedgeofdigitalhealth/

Written by: David ColeIn this episode, experts discuss abdominal aortic aneurysm (AAA), a condition where the main blood vessel in the abdomen weakens and enlarges. They highlight the risks of a ruptured aneurysm, including life-threatening internal bleeding and the need for emergency surgery. The team raises awareness about high-risk groups such as older individuals, men, smokers, and those with a family history, emphasizing the importance of screening programs.

This month on Episode 45 of Discover CircRes, host Cynthia St. Hilaire highlights four original research articles featured in the February 3rd and February 17th issues of Circulation Research. This episode also features an interview with Dr Hind Lal and Dr Tousif Sultan from the University of Alabama at Birmingham about their study Ponatinib Drives Cardiotoxicity by S100A8/A9-NLRP3-IL-1β Mediated Inflammation.   Article highlights:   Pi, et al. Metabolomic Signatures in PAH   Carnevale, et al. Thrombosis TLR4-Mediated in SARS-CoV-2 Infection   Cai, et al. Macrophage ADAR1 in AAA   Koide, et al. sEVs Accelerate Vascular Calcification in CKD   Cindy St. Hilaire:        Hi, and welcome to Discover CircRes, the podcast of the American Heart Association's journal, Circulation Research. I'm your host, Dr Cynthia St. Hilaire from the Vascular Medicine Institute at the University of Pittsburgh, and today I'm going to be highlighting the articles from our February 3rd and 17th issues of Circulation Research. I'm also going to have a chat with Dr Hind Lal and Dr Tousif Sultan from the University of Alabama at Birmingham about their study, Ponatinib Drives Cardiotoxicity by S100A8/A9-NLRP3-IL-1β Mediated Inflammation. But before I get to the interviews, here are a few article highlights.   Cindy St. Hilaire:        The first article I want to highlight comes from the laboratory of Dr Peter Leary at the University of Washington, and the title is Metabolomic Signatures Associated With Pulmonary Arterial Hypertension Outcomes. Pulmonary Arterial Hypertension or PAH is a rare but life-threatening disease in which progressive thickening of the walls of the lung's blood vessels causes increased blood pressure and that increased blood pressure ultimately damages the heart's right ventricle.   Interestingly, progression to heart failure varies considerably among patients, but the reasons why there is variability are not well understood. To find out, this group turned their attention to patient metabolomes, which differ significantly from those of healthy people and thus may also change with severity. Blood samples from 117 PAH patients were analyzed for more than a thousand metabolites by mass spectrometry and the patient's progress was followed for the next three years. 22 patients died within a three-year period and 27 developed significant right ventricle dilation. Other measures of severity included pulmonary vascular resistance, exercise capacity and levels of BNP, which is a metric of heart health. Two metabolic pathways, those relating to polyamine and histidine metabolism, were found to be linked with all measures of severity suggesting a key role for them in disease pathology. While determining how these pathways influence disease as a subject for further study, the current findings may nevertheless lead to new prognostic indicators to inform patient care.   Cindy St. Hilaire:        The next article I want to discuss is coming from our February 3rd issue of Circulation Research and this is coming from the laboratory of Dr Francisco Violi at the University of Rome and the title is Toll-Like Receptor 4-Dependent Platelet-Related Thrombosis in SARS-CoV-2 Infection. Thrombosis can be a complication of COVID-19 and it is associated with poor outcomes, including death. However, the exact mechanism by which the virus activates platelets, which are the cells that drive thrombosis, is not clear. For one thing, platelets do not appear to express the receptor for SARS-CoV-2. They do however, express the TLR4 receptor and that's a receptor that mediates entry of other viruses as part of the immune response. And TLR4 is ramped up in COVID-19 patient platelets. This group now confirms that, indeed, SARS-CoV-2 interacts with TLR4, which in turn triggers thrombosis.   The team analyzed platelets from 25 patients and 10 healthy controls and they found that the platelet activation and thrombic activity were both boosted in the patient samples and could not be blocked using a TLR4 inhibitor. Additionally, immunoprecipitation and immunofluorescent experiments further revealed colocalization between the virus protein and the TLR4 receptor on patient platelets. The team went on to show that the signaling pathway involved reactive oxygen species producing factors p47phox and Nox2, and that inhibition of phox 47, like that of the TLR4 receptor itsel,f could prevent platelet activation. As such, this study suggests that inhibiting either of these proteins may form the basis of an antithrombotic treatment for COVID-19.   Cindy St. Hilaire:        The third article I want to highlight is coming from the lab of Shi-You Chen at University of Missouri and the title of this article is ADAR1 Non-Editing Function in Macrophage Activation and Abdominal Aortic Aneurysm. Macrophage activation plays a critical role in abdominal aortic aneurysm development, or AAA development. Inflammation is a component of this pathology; however, the mechanisms controlling macrophage activation and vascular inflammation in AAA are largely unknown. The ADAR1 enzyme catalyzes the conversion of adenosine to inosine in RNA molecules and thus this conversion can serve as a rheostat to regulate RNA structure or the gene coding sequence of proteins. Several studies have explored the role of ADAR1 in inflammation, but its precise contribution is not fully understood, so the objective of this group was to study the role of ADAR1 in macrophage activation and AAA formation.   Aortic transplantation was conducted to determine the importance of nonvascular ADAR1 in AAA development and dissection and angiotensin II infusion of ApoE knockout mice combined with a macrophage specific knockout of ADAR1 was used to study the role of ADAR1 macrophage specific contributions to AAA formation and dissection. Allograft transplantation of wild type abdominal aortas to ADAR1 haploinsufficient recipient mice significantly attenuated AAA formation. ADAR1 deficiency in hematopoietic stem cells also decreased the prevalence and the severity of AAA and it also inhibited macrophage infiltration into the aortic wall. ADAR1 deletion blocked the classic macrophage activation pathway. It diminished NF-κB signaling and it enhanced the expression of a number of anti-inflammatory microRNAs. Reconstitution of ADAR1 deficient but not wild type human monocytes to immunodeficient mice blocked the aneurysm formation in transplanted human arteries. Together these results suggest that macrophage ADAR1 promotes aneurysm formation in both mouse and human arteries through a novel mechanism of editing the microRNAs that target NF-κB signaling, which ultimately promotes vascular inflammation in AAA.     Cindy St. Hilaire:        The last article I want to highlight is also from our February 17th issue of Circulation Research and it is coming from the lab of Shintaro Mandai at Tokyo Medical and Dental University and the title of the article is Circulating Extracellular Vesicle Propagated MicroRNA signatures as a Vascular Calcification Factor in Chronic Kidney Disease. Chronic Kidney Disease or CKD accelerates vascular calcification in part by promoting the phenotypic switching of vascular smooth muscle cells to osteoblast like cells. This study investigated the role of circulating small extracellular vesicles or SUVs from the kidneys in promoting this osteogenic switch. CKD was induced in rats and in mice by an adenine induced tubular interstitial fibrosis and serum from these animals induced calcification in in vitro cultures of A-10 embryonic rat smooth muscle cells. Intraperitoneal administration of a compound that prevents SEV biosynthesis and release inhibited thoracic aortic calcification in CKD mice under a high phosphorus diet. In Chronic Kidney Disease, the microRNA transcriptome of SUVs revealed a depletion of four microRNAs and the expression of the microRNAs inversely correlated with kidney function in CKD patients.   In vitro studies found that transected microRNA mimics prevented smooth muscle cell calcification in vitro. In silico analyses revealed that VEGF-A was a convergent target of all four microRNAs and leveraging this, the group used in vitro and in vivo models of calcification to show the inhibition of the VEGF-A, VEGFR-2 signaling pathway mitigated calcification. So in addition to identifying a new potential therapeutic target, these SUV propagated microRNAs are a potential biomarker that can be used for screening patients to determine the severity of CKD and possibly even vascular calcification.   Cindy St. Hilaire:        Today I have with me Dr Hind Lal who's an associate professor of medicine at the University of Alabama Birmingham and his post-doctoral fellow and the lead author of the study Dr Tousif Sultan. And their manuscript is titled Ponatinib Drives Cardiotoxicity by S100A8/A9-NLRP3-IL-1β Mediated Inflammation. And this article is in our February 3rd issue of Circulation Research. So thank you both so much for joining me today.   Tousif Sultan:              Thank you.   Hind Lal:                     Thank you for taking time.   Cindy St. Hilaire:        So ponatinib, it's a tyrosine kinase inhibitor and from my understanding it's the only treatment option for a specific group of patients who have chronic myelogenous leukemia and they have to harbor a specific mutation. And while this drug helps to keep these patients alive essentially, it's extremely cardiotoxic. So cardiotoxicity is somewhat of a new field. So Dr Lal, I was wondering how did you get into this line of research?    Hind Lal:                    So I was fortunate enough to be in the lab of Dr Tom Force and he was kind of father of this new area, now is very developed, it's called cardio-oncology. On those days there were basically everything started in cardio-oncology. So I just recall the first tyrosine kinase approved by FDA was in 2000 and that was... Imagine and our paper came in Nature Medicine 2005 and discovering there is... so to elaborate it a little bit, the cancer therapy broadly divided in two parts. One is called non-targeted therapy like chemotherapy, radiations, et cetera, and then there are cytotoxic drugs. So those cytotoxic drugs because they do not have any targeted name on it so they are, cardiotoxic are toxic to any organ was very obvious and understanding. When these targeted therapy came, which is mainly kinase inhibitor are monoclonal antibodies. So these are targeted to a specific pathway that is activated only in the cancer cells but not in any other cells in the body so they were proposed as like magic bullets that can take off the cancer without any cardiotoxity or minimal side effects. But even in the early phase like 2005 to 2010, these came out, these so-called targeted, they are not very targeted and they are not also the magic bullets and they have serious cardiotoxicity.   Cindy St. Hilaire:        And so what's the mechanism of action of ponatinib in the leukemia and how does that intersect with the cardiovascular system?   Hind Lal:                     Yeah, so this is very good question I must say. So what we believe at this point because, so leukemia if you know is driven by the famous Philadelphia chromosome, which is a translicational gene, one part of human chromosome nine and one part of human chromosome 22 and they translocate make a new gene which is BCR-ABL gene. And because it was discovered in Philadelphia UPENN, is named that Philadelphia chromosome, which is very established mechanism, that's how CML is driven. But what we have discovered that the cardiotoxicity driven by totally, totally different from the ponatinib is one of the inflammatory So it's kind of goodening. So this question is so good. One kind of toxicity is called on-target, when toxicity is mediated by the same mechanism, what is the mechanism of the drug to cure the cancer? So in that case your absolute is minimal because if you manipulate that, the drug's ability to cure the cancer will be affected but if the toxicity and the efficacy is driven by two different mechanism, then as in case of ponatinib seems like it's NLRP3 and inflammasome related mechanism. So this can be managed by manipulating this pathway without hampering the drug efficacy on the cancer.   Cindy St. Hilaire:        So what exactly is cardiotoxicity and how does it present itself in these patients?   Hind Lal:                     So these drugs like ponatinib, they call broader CVD effects. So it's not just cardiac, so they also in hypertensives and atherosclerosis and thrombosis, those kind of thing. But our lab is primarily focused on the heart. So that's why in this paper we have given impresses on the heart. So what we believe at this point that ponatinib lead to this proinflammatory pathway described in this paper, which is just 108A9-NLRP3-IL-1β and this inflammatory pathway lead to a cytokine storm very much like in the COVID-19 and these cytokine storms lead to excessive myocarditis and then finally cardiac dysfunction.   Cindy St. Hilaire:        Is the cytokine storm just local in the cardiac tissue or is it also systemic in the patients? Is cardiotoxicity localized only or is it a more systemic problem?   Tousif Sultan:              I would like to add in this paper we have included that we look this cytokine things and explain blood circulation, bone marrow. So the effect is everywhere, it's not local. So we didn't check other organs, maybe other organs also being affected with the ponatinib treatment.   Cindy St. Hilaire:        And what's the initial phenotype of a patient has when they start to get cardiotoxicity, what's kind of like a telltale symptom?   Hind Lal:                     So good thing that in recent years cardio-oncology developed. So initially the patient that were going for cancer treatment, they were not monitored very closely. So they only end up in cardiology clinic when they are having some cardiac events already. So thanks to the lot of development and growth in the cardio-oncology field, now most patients who going for a long-term cancer treatment, they are closely monitored by cardiology clinics.   Cindy St. Hilaire:        Got it. So they can often catch it before a symptom or an event. That's wonderful.   Hind Lal:                     Yeah, so there's a lot of development in monitoring.   Cindy St. Hilaire:        Wonderful. So you were really interested in figuring out why ponatinib induces cardiotoxicity and you mentioned that really up until now it's been very difficult to study and that's because of the limitation of available murine models. If you just inject a wild type mouse with ponatinib, nothing happens really. So what was your approach to finding relatively good murine models? How did you go about that?   Hind Lal:                     So this is the top scientific question you can ask. So like science, the field is try and try again. So initially this is the first paper with the ponatinib toxicity using the real in vivo models. Any paper before this including ours studies published, they were done on the cellular model in hiPSC, that isolated cardiomyocytes. So you directly putting the ponatinib directly the isolated cells. So this is first case when we were trying to do in vivo, maybe other attempt in vivo but at least not published. So first we also treated the animals with ponatinib and that failed, we don't see any cardiotoxic effect. And then when we going back to the literature, the clinical data is very, very clear from pharmacovigilance that ponatinib is cardiotoxic in humans. So when we're not able to see any phenotype in mouse, we realize that we are not mimicking what's happening in the humans.   So we certainly missing something. Now once again I quote this COVID-19, so many people get infected with COVID-19 but people are having preexisting conditions are on high risk to developing CVD. So there was some literature on that line. So we use this very, very same concept that if there is preexisting conditions, so likely who'd have developing future cardiac event will be more. So we use two model in this paper one atherosclerosis model which is APoE null mice mice, another is tag branding which is pressure overload model for the heart and as soon as we start using what we call comorbidity model like patient is having some preexisting conditions and we very clearly see the robust defect of ponatinib on cardiac dysfunction.   Cindy St. Hilaire:        Yeah, it's really, really well done and I really like that you use kind of two different models of this. Do you think it's also going to be operative in maybe like the diabetic mirroring models? Do you think if we expand to other comorbidities, you might also recapitulate the cardiotoxicity?   Hind Lal:                     So you got all the best questions.   Cindy St. Hilaire:        Thank you. I try.   Hind Lal:                     So because this is CML drug and lot of the risk factor for cardiovascular and cancer are common and even metabolic disease. So most of the time these patients are elderly patients and they're having metabolic conditions and most of the time they have blood pressure or something CVD risk factors. So I agree with you, it'll be very relevant to expand this to the diabetes or metabolic models, but these were the first study, we put all our focus to get this one out so news is there then we can expand the field adding additional models et cetera. But I agree with you that will be very logical next step to do.   Cindy St. Hilaire:        Yeah. And so I guess going back to what you know from the human study or the clinical trials or the human observations, are different populations of patients with CML more predisposed to cardio toxicity than others or is that not known yet?   Hind Lal:                     So one other area called pharmacovigilance. So what pharmacovigilance does patient all over the world taking these drugs. So WHO have their own vigilance system and FDA have their own, so it's called BG-Base for the WHO and it's called the FAERS for the FDA. So one can go back in those data sets and see if X patient taking this Y drug and what kind of symptoms or adverse effect they are seeing and if these symptoms are associated with something else. So there is data that if patients having CVD risk factor, they are more prone to develop ponatinib induced cardiac events. But it needs more polish like you asked the just previous question, diabetes versus maybe blood pressure means hypertension, atherosclerosis, or thrombosis. So it has not been delineated further but in a one big bucket if patients are having CVD risk factor before they are more prone and more likely to develop the cardiac events.   Cindy St. Hilaire:        So after you established that these two murine models could pretty robustly recapitulate the human phenotype, what did you do next? How did you come upon the S100A8/A9-NLRP3-IL-1β signaling circuit? How did you get to that?   Hind Lal:                     So in basic science work, whenever we do mouse is called until we get there is cardiac dysfunction, it's called phenotype, right? So mouse had a cardiac phenotype. So next step is, "Why? What is leading to that phenotype?" That's what we call mechanism. So there the best idea to fit the mechanism is using one of the unbiased approaches like you do unbiased proteomics, unbiased RNC analysis, something like this that will analyze the entire transcript like RNC and say, "Okay, these pathway are," then you can do further analysis that will indicate these pathway are different, are altered. So in this case we used RNC analysis and it came out that this yes A8 and yes A9, 100A8 and nine, they were the most upregulated in this whole set. And thereafter we were very lucky. So we started this study at Vanderbilt, where my lab was and thereafter we very lucky to move here and found Sultan who had a lot of experience with this inflammation and immune system and then Sultan may add something on this so he'll be the better person to say something on this.   Tousif Sultan:              So after our RNC analysis, so we got this S100A8 and nine as top hit with the ponatinib treatment. So then we validated this finding with our flow cytometric, qRT PCR aand then we started which pathway is going to release cytokine and all that. So we found that is NLRP3 inflammasome.   Cindy St. Hilaire:        Yeah and well and I guess maybe step back, what is S100A8/A9? What are those? Tousif Sultan:              Yeah, S10A8/A9 is a calcium binding protein. So that's also called alarmin and they basically binds with the pathogen associated pattern and other TLR2 like receptors and then start inflammatory pathway to release cytokine and all that and it's stable in heterodimer form. So S100A8 heterodimer with A9 and then bind with TLR and a start in this inflammatory pathway.   Cindy St. Hilaire:        And what type of cell is that happening in? Is that happening in the immune cells only or is it also in the cardiomyocyte, or...?   Tousif Sultan:              Yeah, we have included all this data. So from where this alarmin is coming with ponatinib treatment, so literature also suggested that neutrophils and monocytes, those cells are the potential to release the alarmin. So here we also found these two type of cells, neutrophils and monocytes. They release huge alarmin with the treatment of ponatinib.   Cindy St. Hilaire:        And so really taking this really neat mechanism to the next level, you then tried attenuating it by using broad anti-inflammatory steroid dexamethasone but also by targeting these specific components, the NLRP and the S100A specific inhibitors and they worked well. It worked really nicely. Does your data show that any of these therapies work better than the other and then are these viable options to use in humans?   Hind Lal:                     Yeah, we have some data in the paper. Are very broad which help a lot in COVID patients, far very acute infections. So in this case, situation is very different cause most of CML patients will going to take ponatinib for lifelong, there is no remission, right? So in those case, its certainly not a very attractive option. We have shown data in the paper that dexamethasone help with the heart but lead to some metabolic changes. So we have compared those with the NLRP3 inhibitors, those metabolic alterations, dexa versus the NLRP3 inhibitors, CY-09. And we demonstrated that targeting is specifically with paquinimod, our NLRP3 inhibitor CY-09, feel better. It can still rescue the cardiac phenotype without having those adverse effect on metabolic parameters.   Cindy St. Hilaire:        That's wonderful. Do you think though that because you have to take ponatinib for life, that long-term NLRP inhibition would also cause problems or...?   Hind Lal:                     So because not every patient who taking ponatinib would develop the cardiac phenotype, right? Which is like a 10%, 12%, patient developing cardiac dysfunction. So I think someone like I strongly believe paquinimod, which is inhibitor of S100A9, will be really good option or at least we have enough data that make us nail for at least a small clinical trial. And we quickly moving on that. At UAB we have our clinical cardio-oncology program and we are already in touch with the director for the clinical cardio-oncology program. So what we trying to do in that small trial is if one of the standard therapy for heart like beta blocker or ARBs inhibitor, is there any preference like one work better than the other in the standard care? So first we doing that project, then we obviously looking forward if one small clinical trial can be done with paquinimod. I strongly believe it should be helpful.   Cindy St. Hilaire:        That is wonderful. And so do you think... There's other chemotherapeutic agents or probably even other non-cancer drugs that cause cardiotoxicity, do you think this mechanism, this pathway, this S100A-NLRP-IL-1β axis is operative in all cardiotoxicities or do you think it's going to be very specific to the ponatinib?   Hind Lal:                     So it's certainly not all, but it'll be certainly more than ponatinib. So in our lab we are using another kinase inhibitor, which is osimertinib and it's not published yet, but now we know that it's also cardiotoxic because it's taking metabolic root or energetics disruption but not this pro-inflammatory part, but we're doing another project which is strep pneumonia induced cardiac dysfunction, which is called pneumonia. So strep pneumoniae, which leads to the pneumonia ,and lot patient die because of the failing heart we see here in the hospitals and we see these pathways operational over there and we gearing up to do clinical trial on that aspect as well, but it's not generalized like all kind of heart will have the same mechanism.   Cindy St. Hilaire:        It's wonderful to see you're already taking those next steps towards really kind of bringing this to a translational/clinical study. So what was the most challenging aspect of this study?   Tousif Sultan:              The challenging aspect, ponatinib is a kinase inhibitor and that was surprising for us how it's activating immune cells. Generally kinase inhibitors, inhibits all the cells like that. So that was challenging. So we repeated it many times did in vitro experiment to confirm that. So we just added, just treated in vitro immune cells with the ponatinib and confirmed it. So that was little challenging.   Cindy St. Hilaire:        So what's next? You mentioned you're going to try some clinical trials, early stage clinical trials. What's next mechanistically, what do you want to go after?   Hind Lal:                     So what we are doing next and we are very, very eagerly trying to do that. So what it was done, we used the cardiac comorbidity models, but as you know, anybody who will take ponatinib will have cancer, right? So we strongly believe that we miss one factor. There was no cancer on these. So that is very logical next step. What that will allow us to do, what rescue experiment we'll have done in this paper. So we saw, "Okay, this rescue the cardiac phenotype, which is taken care of now," but very same time, we not able to demonstrate that this is happening without hurting the cancer efficacy. So if we have the dual comorbid mouse, which have CML a real thing and we have cardiac thing, then that will allow us to demonstrate, "Okay, we got something that can take care of the cardiac problem without hurting the efficacy on the cancer." And it will be best if you also help little bit to more potentiate the cancer efficacy.   Cindy St. Hilaire:        Yes. Excellent. Well, congratulations on a beautiful study, really exciting findings. Dr Lal and Dr Sultan, thank you so much for taking the time to talk with me today.   Tousif Sultan:              Thank you so much.   Hind Lal:                     Well thank you, Cynthia. We really appreciate your time. Thank you for having us.   Cindy St. Hilaire:        Yeah, it was great.   Cindy St. Hilaire:        That's it for our highlights from the February 3rd and February 17th issues of Circulation Research. Thank you so much for listening. Please check out the Circulation Research Facebook page and follow us on Twitter and Instagram with the handle @CircRes and #DiscoverCircRes. Thank you to our guests, Dr Hind Lal and Dr Tousif Sultan. This podcast is produced by Ishara Ratnayake, edited by Melissa Stoner and supported by the editorial team at Circulation Research. Some of the copy text for the highlighted articles was provided by Ruth Williams. I'm your host, Dr Cynthia St. Hilaire, and this is Discover CircRes, you're on-the-go source for most exciting discoveries in basic cardiovascular research. This program is copyright of the American Heart Association 2023. And the opinions expressed by the speakers in this podcast are their own and not necessarily those of the editors or of the American Heart Association. For more information, please visit ahajournals.org.  

In this episode, we review the high-yield topic of Abdominal Aortic Aneurysm from the Cardiovascular section. Follow Medbullets on social media: Facebook: www.facebook.com/medbullets Instagram: www.instagram.com/medbulletsofficial Twitter: www.twitter.com/medbullets --- Send in a voice message: https://anchor.fm/medbulletsstep1/message

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.24.517638v1?rss=1 Authors: Nemade, H. N., Mehrkens, D., Lottermoser, H. S., Yilmaz, Z. E., Schelemei, P., Picard, F. R., Geissen, S., Schwab, G. F., Hoyer, F. F., Guthoff, H., Hof, A., Nettersheim, F. S., Sachinidis, A., Winkels, H., Baldus, S., Pasparakis, M., Adam, M., Mollenhauer, M. Abstract: Background: Receptor-interacting serine/threonine-protein kinase 1 and 3 (RIPK1 and RIPK3) dependent cell death has been identified as a crucial mediator of abdominal aortic aneurysm (AAA) development. RIPK3 mediates phosphorylation of Mixed lineage kinase domain like pseudokinase (MLKL) thereby inducing its oligomerization and translocation to the cell membrane. Given the dual role of RIPKs being involved in necroptosis as well as in apoptosis induction, the specific role of MLKL-induced necroptotic cell death in AAA remains unclear. Methods: We monitored elastase-perfusion (PPE) induced progression of AAA in C57BL/6N (WT), RIPK1 kinase deficient (Ripk1D138N/D138N), MLKL knockout (Mlkl-/-) and MLKL phosphodeficient (MlklAA) mice by ultrasound measurements, histological analyses and bulk mRNAseq techniques to assess structural and molecular aortic changes. Bone marrow transplantation studies in WT and MlklAA mice were utilized to dissect the role of MLKL in smooth muscle cells (SMCs) and myeloid cells in AAA development. MLKL expressing human SMCs were generated to investigate necroptosis-induced proinflammatory cytokine secretion and subsequent polymorphonuclear neutrophil (PMN) migration and activation in vitro. Results: Ultrasound analysis showed that ~70% of the WT animals developed PPE induced-AAA with significant aortic structural alterations and enhanced myeloid cell infiltration. In contrast, Ripk1D138N/D138N, MlklAA, and Mlkl-/- mice were protected from AAA. This protection was associated with reduced adverse extracellular matrix (ECM) remodeling and leukocyte infiltration. MLKL deficiency was associated with a significant downregulation of genes involved in fibrinolysis, anti-inflammatory response, immune response and complement activation in aortic tissue in AAA. Bone marrow transplantation studies showed the lack of MLKL in SMCs to be the main driver of AAA protection. Proinflammatory cytokine secretion was elevated in necroptosis induced SMCs and resulted in a significant accumulation and activation of PMN. Conclusions: Overall, these findings indicate that MLKL-induced necroptotic SMC death and subsequent proinflammatory leukocyte activation plays a causative role in AAA development and suggests that pharmacological inhibition of MLKL may represent a promising treatment strategy for AAA disease. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2022.11.23.517652v1?rss=1 Authors: Metz, L. M., Feige, T., de Biasi, L., Ehrenberg, A., Mulorz, J., Toska, L. M., Reusswig, F., Quast, C., Gerdes, N., Kelm, M., Schelzig, H., Elvers, M. Abstract: Abdominal aortic aneurysm (AAA) is a common disease and highly lethal if untreated. The progressive dilatation of the abdominal aorta is accompanied by degradation and remodeling of the vessel wall due to chronic inflammation. Pannexins represent anion-selective channels and play a crucial role in non-vesicular ATP release to amplify paracrine signaling in cells. Thus, pannexins are involved in many (patho-) physiological processes. Recently, Panx1 channels were identified to be significantly involved in AAA formation through endothelial derived Panx1 regulated inflammation and aortic remodeling. In platelets, Panx1 becomes activated following activation of glycoprotein (GP)VI. Since platelets play a role in cardiovascular diseases including AAA, we analyzed the contribution of platelet Panx1 in the progression of AAA. We detected enhanced Panx1 plasma levels in AAA patients. In experimental AAA using the pancreatic porcine elastase (PPE) mouse model, a major contribution of platelet Panx1 channels in platelet activation, pro-coagulant activity of platelets and platelet-mediated inflammation has been detected. In detail, platelets are important for the migration of neutrophils into the aortic wall induced by direct cell interaction and by activation of endothelial cells. Decreased platelet activation and inflammation did not affect ECM remodeling or wall thickness in platelet-specific Panx1 knock-out mice following PPE surgery. Thus, aortic diameter expansion at different time points after elastase infusion of the aortic wall was unaltered in platelet-specific Panx1 deficient mice suggesting that the modulation of inflammation alone does not affect AAA formation and progression. In conclusion, our data strongly supports the role of platelets in inflammatory responses in AAA via Panx1 channels and adds important knowledge about the significance of platelets in AAA pathology important for the establishment of an anti-platelet therapy for AAA patients. Copy rights belong to original authors. Visit the link for more info Podcast created by Paper Player, LLC

Thanks Dr Siak for the fantastic exam session!Check out all my resources below and the final exam course for more examples of worst case scenarioshttps://anaesthesia.thinkific.com/courses/FinalExamViva StemYou are asked to review a 76-year-old man for planned abdominal aortic aneurysm (AAA) repair on your list in seven days' time. His aneurysm extends above the renal arteries. ¤He has a background of hypertension, type 2 diabetes mellitus and a transient ischaemic attack (TIA). He has a body mass index of 32 kg/ m2 and has a 24 pack-year history of smoking.He is a Jehovah's Witness.His medications include ¤clopidogrel 75mg daily ¤rosuvastatin 10mg daily ¤perindopril 4mg mane ¤metoprolol 25mg bd ¤metformin 1000mg bd What is his risk of renal impairment perioperatively?What criteria can be used to define acute kidney injury ---------Find us atInstagram: https://www.instagram.com/abcsofanaesthesia/Twitter: https://twitter.com/abcsofaWebsite: http://www.anaesthesiacollective.comPodcast: ABCs of AnaesthesiaPrimary Exam Podcast: Anaesthesia Coffee BreakFacebook Page: https://www.facebook.com/ABCsofAnaesthesiaFacebook Private Group: https://www.facebook.com/groups/2082807131964430---------Check out all of our online courses and zoom teaching sessions here!https://anaesthesia.thinkific.com/collectionshttps://www.anaesthesiacollective.com/courses/---------#Anesthesiology #Anesthesia #Anaesthetics #Anaesthetists #Residency #MedicalSchool #FOAMed #Nurse #Medical #Meded ---------Please support me at my patreonhttps://www.patreon.com/ABCsofA---------Any questions please email abcsofanaesthesia@gmail.com---------Disclaimer: The information contained in this video/audio/graphic is for medical practitioner education only. It is not and will not be relevant for the general public.Where applicable patients have given written informed consent to the use of their images in video/photography and aware that it will be published online and visible by medical practitioners and the general public.This contains general information about medical conditions and treatments. The information is not advice and should not be treated as such. The medical information is provided “as is” without any representations or warranties, express or implied. The presenter makes no representations or warranties in relation to the medical information on this video. You must not rely on the information as an alternative to assessing and managing your patient with your treating team and consultant. You should seek your own advice from your medical practitioner in relation to any of the topics discussed in this episode' Medical information can change rapidly, and the author/s make all reasonable attempts to provide accurate information at the time of filming. There is no guarantee that the information will be accurate at the time of viewingThe information provided is within the scope of a specialist anaesthetist (FANZCA) working in Australia.The information presented here does not represent the views of any hospital or ANZCA.These videos are solely for training and education of medical practitioners, and are not an advertisement. They were not sponsored and offer no discounts, gifts or other inducements. This disclaimer was created based on a Contractology template available at http://www.contractology.com.

Name of Surgery: Endovascular Aortic Aneurysm Repair (Infrarenal)   In today's episode of our Holding Pressure (HP) Series, developed by medical students for medical students, Janhavi and Andrew review the basics of endovascular abdominal aortic aneurysm repair (EVAR). Authors:  Janhavi Nikhil Patel is a third and final year medical student at McMaster University. She previously completed her undergraduate in Physiology from Western University.  Andrew Lazar (@Lazar_andy) is a PGY-4 General Surgery resident at Morristown Medical Center in New Jersey. He completed a T32 research fellowship in vascular surgery at Columbia University. He graduated from Weill Cornell Medicine. Editor: Yasong Yu Reviewers: Imani McElroy and Amanda Fobare Core Resource: Rutherford's Vascular and Endovascular Therapy 9th Edition Chapter#69, 70, 72, 73 Additional Resources: EVAR-1 Trial - Endovascular versus Open Repair of Abdominal Aortic Aneurysm. N Engl J Med, 362 (20) (2010), pp. 1863-1871, Endovascular versus Open Repair of Abdominal Aortic Aneurysm | NEJM OVER Trial - F.A. Lederle, T.C. Kyriakides, K.T. Stroupe, J.A. Freischlag, F.T. Padberg, J.S. Matsumura, et al. Open versus endovascular repair of abdominal aortic aneurysm. N Engl J Med, 380 (2019), pp. 2126-2135. Open versus Endovascular Repair of Abdominal Aortic Aneurysm | NEJM Relevant Audible Bleeding episodes Landmark Papers - IMPROVE VSITE Review - AAA Endovascular Aortic Repair Preoperative Sizing VSITE Review - Vascular Access For a full outline check out our website. Calling all medical students Submit your questions for the mailbag episode! Ask us any question related to vascular surgery, and have it answered on the podcast.  Include the following Your name, school, and year Who do you want to address the question to (resident, fellow, attending, or someone specific) Send them in writing or voice-recorded format.   Send to audiblebleeding@vascularsociety.org. Please share your feedback through our Listener Survey! Follow us on Twitter @audiblebleeding Learn more about us at https://www.audiblebleeding.com/about-1/ and #jointheconversation.

Daily Cardiology Symposium 1401: Peripheral vascular diseases

Take Home Points Consider AAA in patients with acute onset of back or abdominal pain particularly in patients > 50 and in those with a history of hypertension Consider ruptured AAA in patients (especially those > 50 years of age) with unexplained hypotension, back or abdominal pain All ruptured AAAs should be considered unstable regardless ... Read more The post REBEL Core Cast 82.0 – Abdominal Aortic Aneurysm appeared first on REBEL EM - Emergency Medicine Blog.

Dear friends, we prepared an episode about TAA and AAA and we discuss the general principles of these two diagnoses, you can also download the slides via this link:http://ecardiocast.com/wp-content/uploads/2022/03/acute-aortic-syndrome.pdf

With more and more EVAR comes more and more endoleaks. But when do they matter and what can/should we do about them? In this episode, we present a case of a stubborn endoleak and use the course to illustrate a simple path towards the management of endoleaks following endovascular aneurysm repair. Dr. Nicholas Osborne is an Associate Professor of Vascular Surgery at the University of Michigan and the Chief of Vascular Surgery at the Ann Arbor Veteran's Affairs Healthcare System. Dr. Frank Davis is a Chief Resident in the Integrated Vascular Surgery program at the University of Michigan. Dr. Craig Brown is a PGY-6 in the General Surgery program at the University of Michigan. Guidelines around Endoleak Management Society for Vascular Surgery Practice Guidelines on the Care of Patients with an Abdominal Aortic Aneurysm: https://pubmed.ncbi.nlm.nih.gov/29268916/ Conservative Management of Type II Endoleaks: https://pubmed.ncbi.nlm.nih.gov/25042332/ Please visit behindtheknife.org to access other high-yield surgical education podcasts, videos and more.  

Surprising case that initially sounded like septic shock, but upon further investigation, the patient had a huge abdominal aortic aneurysm that was dissecting.  Learn about the clinical presentation, emergent interventions, and the nurse's role in saving this patient's life. 

An aneurysm is a stretched out blood vessel that can lead to complications if ruptured. Aneurysms are caused by smoking and certain genetic factors. Vascular surgeon Dr. Claire Griffin talks through the most common type of aneurysms, an abdominal aortic aneurysm. Find out how they're detected and if you're at risk.

In this episode, we review the high-yield topic of Abdominal Aortic Aneurysm from the Cardiovascular section.

Dr Carolyn Lam: Welcome to Circulation on the Run! Your weekly podcast summary and backstage pass to the journal and its editors. We're your co-hosts, I'm Dr. Carolyn Lam, Associate Editor from the National Heart Center and Duke National University of Singapore. Dr. Greg Hundley: I'm Greg Hundley, Associate Editor, Director of the Pauley Heart Center, VCU Health in Richmond, Virginia. Dr Carolyn Lam: Greg, we got double features today. Now, the first one's all about fruit and vegetables. Now, before you switch off, this is a very important one, okay? So, listen on. And the second is on the EMBRACE heart failure trial. Now, this was a late breaker, very important, more data on empagliflozin, that SGLT2 inhibitor. So really, really fun discussions coming right up. But first, can I dig into one of the papers that I'm really dying to tell you about? Dr. Greg Hundley: Absolutely. Dr Carolyn Lam: Okay. This is all about the diagnostic performance of high-sensitivity cardiac troponin T strategies, that super hot topic. We know that European data support the use of low high sensitivity troponin measurements or a 0/1 hour algorithm for myocardial infarction or to exclude MACE among emergency department patients with possible acute coronary syndrome. However, there's really very modest U.S. data to validate these strategies. This study today from Dr. Allen and colleagues from University of Florida, really evaluated the diagnostic performance of an initial high sensitivity cardiac troponin T measure below the limit of quantification. And that is six nanograms per liter, a 0/1 hour algorithm, and their combination with heart scores for excluding MACE in a multi-site U.S. cohort. And this is the largest prospective multi-site U.S. study of high sensitivity troponin T strategies to date. Dr. Greg Hundley: Wow, Carolyn you've really piqued my interest. So what did they find? Dr Carolyn Lam: Okay. And initial high sensitivity, cardiac troponin T below that level of quantification of six nanograms per liter was associated with a negative predictive value of 98.3% for 30-day MACE. Okay. That was that value itself. Now the 0/1 hour algorithm rolled out 57.8% of patients with a negative predictive value of 97.2% for 30-day MACE. The addition of a low-risk heart score to that initial high sensitivity troponin T level below that six nanogram per liter and the 0/1 hour algorithm improved the negative predictive value for 30-day MACE to 99% and 98.4% respectively. Dr. Greg Hundley: Wow. Carolyn, it looks like a really comprehensive analysis of the high sensitivity troponin. So tell us what are the clinical implications of this study? Dr Carolyn Lam: So these data seem to imply that when used without a risk score and initial high sensitivity troponin T below six nanograms per liter, or a 0/1 one hour algorithm, may not have sufficient sensitivity or negative predictive value to exclude 30-day MACE in the U.S emergency department patients. But the addition of that low-risk heart score to those measures improves the negative predictive value, but rolls out fewer patients. And so in totality, these results suggest that in the U.S. Emergency departments, adding a risk score to either of these strategies really increases their safety. Dr. Greg Hundley: Boy, great new information in our journal. Well, Carolyn, I'm going to switch to the world of basic science and start to evaluate in this next paper, the regulation of cellular signatures in children with dilated cardiomyopathy, and the work comes to us from Dr. Stephanie Dimmeler from Goethe University in Frankfurt. So Carolyn, Stephanie's team performed single nuclei RNA sequencing with heart tissues from six children with dilated cardiomyopathy. One was age 0.5, 1.75 and another at 5, 6, 12, and then 13 years of age. And they did this to gain insight into age and disease-related pathophysiology, pathology, and molecular fingerprints. And the goal was to gain further insight into dilated cardiomyopathy, which is a leading cause of death in children with heart failure. Dr Carolyn Lam: Cool. So what did they find Greg? Dr. Greg Hundley: Right, Carolyn. So, the number of nuclei in fibroblast clusters increased with age in dilated cardiomyopathy patients, a finding that was consistent with an age-related increase in cardiac fibrosis quantified by cardiovascular magnetic resonance imaging. Dr. Greg Hundley: Now Carolyn, fibroblast of the dilated cardiomyopathy patients over six years of age showed a profoundly altered gene expression pattern with enrichment of genes encoding fibrillary collagens, modulation of proteoglycans and a switch in thrombospondin isoforms and signatures for fibroblast activation. Additionally, Carolyn, a population of cardiomyocytes with a high pro-regenerative profile was identified in infant dilated cardiomyopathy patients, but was absent in those children that were greater than six years old. And this cluster in these infants showed high expression of cell cycle activators, such cyclin D family members increased glycolytic metabolism and any oxidative genes and alterations in beta adrenergic signaling genes. Dr Carolyn Lam: Wow. That sounds like a magnificent and elegant study. Could you boil it down to the take home messages? Dr. Greg Hundley: You bet. Carolyn. Great question. So two points first, infants with a predominantly regenerative cardiomyocyte profile, may preferentially receive treatment strategies to support cardiac regeneration while patients with a pattern associable with cardiac fibrosis may benefit from an early anti-fibrotic therapy to avoid diastolic dysfunction. And second, despite the impracticality of performing these large cohort studies in children with dilated cardiomyopathies, tailored pharmacological treatment is possibly realistic. For example, based on the expression of beta adrenergic signaling genes. Dr Carolyn Lam: Oh wow. That is super cool. That's Circulation for you, publishing these amazing basic science papers with very big clinical implications. Well, I've got another basic science paper for you and this time I've learned a new word actually. It's called O-GlcNAcylation. I should get you to say it after me. I had to get our editor-in-chief Joe Hill to teach me to say that, O-GlcNAcylation. So, cardiomyopathy from diverse causes is marked by increased O-GlcNAcylation. Now, in this paper, co-corresponding authors, Dr. Anderson and Umapathi from Johns Hopkins University provide a new genetic mouse model to control myocardial O-GlcNAcylation independent of pathological stress. Their data actually provided evidence that excessive O-GlcNAcylation caused cardiomyopathy, at least in part due to defective energetics. Enhanced O-GlcNAcase activity was well-tolerated. And conversely, attenuation of O-GlcNAcylation was beneficial against pressure overload induced pathological remodeling in heart failure. Dr. Greg Hundley: Interesting, Carolyn. So what are the clinical implications of these findings? Dr Carolyn Lam: Well, the data really provide new proof of concept that excessive O-GlcNAcylation is sufficient to cause cardiomyopathy, and they also suggest that attenuation of this excessive O-GlcNAcylation may represent a novel therapeutic approach for cardiomyopathy. Dr Carolyn Lam: Shall we go on and sort of wrap up on what else is in this issue? Because I'd like to talk about highlights from the Circulation family of journals that Sarah O’Brien really beautifully summarizes, talking about everything from Circulation: Arrhythmia & Electrophysiology, to [Circulation:] Cardiovascular Quality & Outcomes. It's just a beautiful piece where we get all the highlights. Must read. There's also a Perspective piece by Dr. Gillis on Rhythm Control in Atrial Fibrillation: Is Earlier the Better?, and that discusses the EAST-AFNET 4 and early AF trials. Dr. Greg Hundley: Very good, Carolyn. Well, from the mailbox, professors Pan and Liu exchange letters regarding a prior response to a letter regarding the article Genetic Architecture of Abdominal Aortic Aneurysm in the Million Veteran Program. Also, Dr. Arbus-Redondo has an EKG challenge entitled, Dual Chamber Pacemaker after Sinus Node Dysfunction and an Enlarged Right Atrium. Is it what it seems? Dr. Greg Hundley: And then finally, Dr. Corrado has a very nice Research Letter, entitled, Serial versus Single Cardiovascular Screening of Adolescent Athletes. Dr. Greg Hundley: Well, Carolyn, I'm dying to hear about fruits and vegetables. How about we get onto those featured discussions? Dr Carolyn Lam: Cheeky, cheeky, Greg. Here we go. Dr Carolyn Lam: Oh, I'm so excited about today's featured discussion because it's about my favorite thing, fruits and vegetables. Okay, wait a minute, everybody. Before you start rolling your eyes, this is a really important one. Have you ever asked yourself, what is the optimal intake levels of fruit and vegetables for maintaining long-term health? Well, guess what? We're about to find out and I'm so pleased to have the first author of today's feature paper, Dr. Wang Dong, and he's from Harvard medical school and Brigham Women's Hospital. We also have our Associate Editor, Dr. Mercedes Carnethon from Northwestern University and our Associate Editor who is also the editorialist to this paper, Dr. Naveed Sattar from University of Glasgow. So welcome, everyone. Dr. Wang, please tell us what you did in this study and what were your main results? Dr. Wang Dong: Thank you, Carolyn. So, basically, in this study, we analyzed the data from two long running cohort study. That is the Nurses' Health Study and Health Professional Follow-Up Study. So these two study includes more than 100,000 participants who had been followed for up to 30 years. And we also include a meta-analysis that includes in total 26 studies and about two million participant from 29 countries, and had countries around the world. So, basically, the major finding from this study is, of course, the intake of fruits, vegetable is inversely associated with the risk of death from all cause and the different kinds of cause-specific mortality. And we have a very interesting finding that is intake of about five servings per day, that can be translated into two serving of fruits and three servings of vegetables per day, was associated with the lowest risk of total mortality. So that's an optimal intake level for fruits and vegetable. Dr. Wang Dong: And another important finding from this study is, not all foods that some people consider to be fruits and vegetables can offer the same health benefits. For example, in this study, we found that starch vegetables such as peas and corn, and some fruits juice and potatoes are actually not associated with any benefit in terms of longevity. On the other hand, if you look at green living vegetables such as spinach, kale, and fruits that's orange color fruits and vegetables, that's rich in beta-carotene and vitamin C such as citrus fruits and berries, carrots they're associated with a substantial reduction in the risk of total mortality. That's a major finding from this paper. Dr Carolyn Lam: Oh, I just love it. I mean, just like such wholesome, beautiful findings from a wonderful study. Now, if I could ask you, cause I think the first thing everyone's going to say is, okay, these are associations. I mean, what'd you do about the residual risks? Could you maybe describe how you try to address some of these things like, is taking in fruits and vegetables just a surrogate for people who, I don't know, exercise more, for example? Dr. Wang Dong: Yeah. So in original data analysis, we actually have extensive data collection of all kinds of foods, lifestyle, risk factors, medication use, any health-related variables. So we carefully adjust for a large number of confounding factors. So actually another thing I want to point out, most all of these health-related lifestyle factors actually are inverse confounding factors in this kind of analysis. So when you adjust for other confounding factors, it's tend to attenuated your inverse association. So the review from confounding actually wouldn't be a major explanation for this association. Dr Carolyn Lam: Oh, that's great. And by the way, I think I misspoke. I'm not sure if I said residual confounding or residual risk just now, but you absolutely read me right, that I meant residual confounding. So thanks. Now that we've got that out of the way, if I could ask Mercedes, please. I mean, ah, another fruits and vegetables paper, I mean, what made this one different that we said we have to have it at Circulation. Dr Mercedes Carnethon: Well, thanks so much, Carolyn. And thank you Dong, for your team's outstanding work. I know what excited me about it was the demonstration of something that we have adopted into our lexicon, that one needs five fruits and vegetables. So I was excited to see you quantify it. In particular, the question I have for you is, did you see that these patterns of association of fresh fruit and vegetable intake were consistent across the age range and in both sexes? Dr. Wang Dong: Yes, of course. In total, this acts as a stratification variable. So basically, in our original data analysis, we did the analysis in the Nurses' Health Study, which all the participants are women, and in the Health Professional Follow-Up study, in which all the participants are men, would be analyzed separately and we found very consistent results in both cohorts. Then will be the meta-analysis to meta-analyze the results from these two cohorts. It comes out age, actually if you look at the paper, I think in one of the supplemental table, with the age stratified analysis, to look at the a better association if it still holds in different age group. And we did found that the results is pretty consistent in different age groups. And also, I would point out this meta-analysis provides further support to show that this results is generalizable in different people with different social economic status, demographics status also from different background. Dr Mercedes Carnethon: Thank you so much, Dong. it brings me to what Naveed wrote about in his editorial, that food is medicine and I just really loved that and loved the implications of that. So, I don't know, Naveed, if you've got some comments to make? Questions? Dr Naveed Sattar: Yeah, thanks Mercedes. No, I really love this as well because clearly the cardiovascular community, we do lots of trials. Lots of us are nihilists and just look at trials, but actually it's hard to do trials in the food and the dietary area, but these data are very consistent. I think there are multiple potential mechanisms that may explain this. We all have to eat every day, so it's a big part of our lives. Increase fiber intake, increase potassium, micronutrients, food displacement, the more fruit and veggies you eat, the less you'll eat of other things that perhaps are not as protective. And actually, part of the motivation to write an editorial was to put all that into context in terms of mechanisms. And particularly fiber, I think we underestimate the importance of fiber, but then it was also to discuss, well, if this is true, how do we help people make the changes? Dr Naveed Sattar: And at the level of policy, at the level of high risk groups, and my own particular favorite is really communicating dietary change in the clinic. And one of the things I often try, and we put this in a kind of headline figure in the editorial, was actually getting people to try to undergo the palate test or the retraining their palates. I have lots of patients, who, would you believe, in the west of Scotland, never really eat fruit and veg, and I really pushed them to say, "Look, would you please try? And it might take a few weeks for you to retrain your palate". And lots of people come back saying, "Ah, you're correct. And my God, now I like banana and I now like salad." Dr Naveed Sattar: So actually, there's lots of tips that we can do to help people increase from their average of two to three intake, which is the vast majority of population, to four to five, but it's a gradual process and it requires good communication with our patients and to compel them that these changes might take time, but that if they make these changes, they can get to a point where they really enjoy eating fruit and veg and all the multiple health benefits that come, which this paper has now showed, Mercedes. Dr Naveed Sattar: I think for me, that was the real nub of this. Dr Carolyn Lam: Naveed, I just love the way you express it. And indeed, everyone take up that editorial and look at that beautiful figure. I love the colorful fruits and vegetables on top because it also reminds us, and this paper shows, we are not talking about potato chips, and was it those, corn and peas. But, you know, we're talking about nutrition and fiber and the good stuff. Oh, this is just amazing. I wish we could go on forever, but we have a double feature this issue. And I just want to end by saying, thank you, thank you all of you, for being on the show today. It was such an important topic and I really loved the discussion as I'm sure the audience did. Thank you. Dr Mercedes Carnethon: Thank You. Dr Naveed Sattar: Thanks very much. Dr. Wang Dong: Thank you so much. Dr Carolyn Lam: I am so pleased to have with us today, a friend, a deeply admired colleague and the corresponding author of today's feature discussion, Dr. Mikhail Kosiborod from Saint Luke's Mid America Heart Institute. Dr Carolyn Lam: Welcome, Mikhail. And thank you for publishing this beautiful paper on EMBRACE heart failure with us. I know that this was presented as a late-breaking trial at the Heart Failure Society of America meeting, and it's a very much anticipated paper, but maybe I could start with it's all about SGLT2 inhibitors these days. So please tell us how does EMBRACE add to this accumulating knowledge that we have on SGLT2 inhibitors and heart failure? Dr. Mikhail Kosiborod: Well, first of all, Carolyn, thanks so much for publishing our trial in Circulation. And you're right, SGLT2 inhibitors have been taking the world of cardiometabolic medicine and heart failure by storm over the past few years. EMBRACE is a very unique trial because it really, took this world of rapidly developing technology in heart failure and heart failure monitoring, and coupled it with one of the hottest topics in heart failure today in terms of drug management, which is the advent of SGLT2 inhibitors and the emergence SGLT2 inhibitors as a efficacious therapy, not just for prevention of heart failure, but also treatment of heart failure. Because as you know, pulmonary artery pressure and hemodynamic status are one of the strongest predictors of patient outcomes, both in terms of symptoms, hospitalizations, and deaths in heart failure. And we know actually that monitoring and intervening on elevated pulmonary pressure in this patient population may lead to hospitalizations and possibly even death. Dr. Mikhail Kosiborod: But up until recently, it's been very difficult to monitor pulmonary pressures and to use them as an outcome in heart failure trials, because you will have to use invasive monitoring, essentially a right heart catheterization to get that data. Well, now we can actually have this implanted sensors like CardioMEMS, which are the sensors that we use in EMBRACE-HF trial. So, the question we wanted to ask is, we know SGLT2 inhibitors in DAPA-HF and EMPEROR-Reduced trials, clearly reduce the risk of cardiovascular death and hospitalization for heart failure, worsening heart failure, but the mechanisms have been hotly debated. Is there a possibility these agents can actually have an impact on hemodynamic status and pulmonary pressures? And that's the key central question that we tried to address and EMBRACE-HF trial by using this novel technology at the time, now it's been around for a few years, to noninvasively measure pulmonary pressures and use it as a primary outcome in our trial. Dr Carolyn Lam: Mikhail, first of all, hats off, it was a very, very clever idea to look at these patient populations who already have CardioMEMS right, and then perform this randomized trial. I mean, when I saw this, I was like, "Aw, man, how come I didn't think of that? That's just like so clever, but it's just so Mikhail to be ahead of the curve." But I'd like to remind the audience, this was a prospective randomized trial, the pre-specified outcomes, right? So maybe you could describe that in a greater detail and then the results. Yeah. Dr. Mikhail Kosiborod: Absolutely. Well, Carolyn, first of all, once again, thank you very much. You're being very kind. We do think it was a very novel clever idea and that you're absolutely correct, as this was very rigorously designed, randomized, double blind placebo controlled investigating trial within this study and 10 sites in United States. And the patients had to have heart failure, either with reduced or preserved ejection fraction, about half-and-half actually, as it turned out to be once it's all said and done with the trial. Because they had to have implanted CardioMEMS for clinical indication previously, they were quite advanced in terms of their heart failure. So more than half of the patients were in NYHA class III or IV, they had elevated brain natriuretic peptide levels, they had hybrid symptoms as you would expect. And essentially the patients were screened, and if they were eligible, randomized to use a empagliflozin-placebo in a double-blind fashion. Dr. Mikhail Kosiborod: And they were monitored actually for a couple of weeks prior to randomization to get a baseline pulmonary artery diastolic pressure. They were then treated for 12 weeks with empagliflozin, 10 milligrams a day, or a matching placebo. And we were measuring pulmonary pressure twice a day, every day for the 12 week treatment period, and then at the end of the treatment period, the treatment was stopped, but we actually continued to measure pulmonary pressure for one additional week again, twice a day, every day. So we actually saw what happened for one week after the treatment was stopped. And, as I mentioned before, the patient population was quite advanced from a heart failure standpoint. These were patients that were adequately managed with guideline-directed medical therapy for heart failure. Of course, about half of those patients have, have HFpEF. Did I mention before was the standard of care is not a thoroughly defined? Dr. Mikhail Kosiborod: And essentially what we observed was quite remarkable, which is average pulmonary artery diastolic pressure at baseline was about 22 millimeters of mercury across the patient population, and in patients treated with empagliflozin, there was quite a rapid reduction in pulmonary artery diastolic pressure that we saw almost immediately within one week as compared with placebo. And that divergence of curves in terms of pulmonary artery diastolic pressure continued over the entire 12-week treatment period. And by the end of the treatment period, there was nearly two millimeter of mercury difference in favor of empagliflozin, with lower pulmonary artery diastolic pressure in patients with empagliflozin compared with placebo. And also interestingly, even after the treatment was stopped for an additional week, those curves continued to diverge, with even greater lowering of pulmonary artery diastolic pressure in patients that received empagliflozin. So, I think to our knowledge, this is the first evidence from a randomized clinical trial, randomized double blind placebo controlled clinical trial, that SGLT2 inhibitors, in this case, empagliflozin, have essentially direct the congestion effect towards a lower pulmonary artery pressure rapidly and with effect amplified over time. Dr Carolyn Lam: Yes. Congratulations and beautifully present it there. Now, if I could ask a few more questions now, because the things will come up there. What happened to the diuretic dose? Is this depend on diuretic dose? Are there any subgroups that appeared to benefit more? Dr. Mikhail Kosiborod: No, excellent question, Carolyn. So first of all, we monitored average daily furosemide equivalent dose continuously throughout the trial, and what we observed was that there was no difference in diuretic dose, essentially, between the two groups from a loop diuretic management standpoint. Now, remember this patients are getting frequent pulmonary pressures with diuretics being adjusted all the time. But if you look at what happens over time, that's one of the figures in the paper you see essentially the flat lines in both groups. And coupling that with the fact that pulmonary pressures continue to diverge for another week after the treatment was stopped, at least in my mind, suggests that this hemodynamic benefits as we observed with empagliflozin as compared with placebo was lowering of pulmonary pressures is likely not simply due to diuretic effect. It just cannot be explained only by diuretic effect. I think these findings are very much in line with the analysis that we had in DAPA-HF trial with the analysis that recently were published from EMPEROR-Reduced, showing that you just can't explain what you see with heart failure benefits with SGLT2 inhibitors simply by diuresis. Dr Carolyn Lam: Fascinating. Well, how about the question of diabetes? Dr. Mikhail Kosiborod: Yes. So in terms of subgroups, that you mentioned, we did do subgroup analysis. Now I will say that the subgroup analysis have to be interpreted with a great deal of caution in this trial, because the entire trial had about 65 patients, so it's a small trial. It was really powered to look at the entire patient population and look at the primary end point of the diastolic pressure. Nevertheless, as I mentioned before, we had half-and-half reduced and preserved EF and we did not see a statistically significant heterogeneity in the treatment effect when we look at patients with reduced to preserved EF, so that hopefully both for outcome trials in preserved EF heart failure, we'll see, of course, what happens with that. And in terms of diabetes we saw a bit greater effect in patients with diabetes as compared to patients without diabetes, in terms of pulmonary artery pressure reduction. Dr. Mikhail Kosiborod: But again, I would just strongly caution interpretation of those subgroups because certainly when we look at clinical outcomes in those DAPA-HF and EMPEROR-Reduced, we see no such difference. We see that the benefits, right, the hard clinical outcomes, benefits, are quite consistent regardless of diabetes status. I will say one other thing, which I think is really important. If you look at the pulmonary artery pressure trajectory in patients treated with placebo in EMBRACE-HF, you see that they actually go up over time. And this is in patients that have frequent monitoring of blood pressures, our own guideline-directed medical therapy are closely watched by predominantly heart failure cardiologists and their teams to make sure that they're well-managed. And despite that, you see this increase in pulmonary pressure over time, and that's just another reminder to us that heart failure is a progressive disease despite best available therapy. Dr. Mikhail Kosiborod: These patients deteriorate over time, which is why treatment, novel advancements, treatments like SGLT2 inhibitors and their effective implementation is just so important because we know the benefits occur very early. We saw one week here, when we start seeing separation of curves, certainly see a significant difference by 12 weeks with pulmonary pressure. But of course we know with clinical outcomes, we see within a few weeks of randomization, already a significant benefit in reducing CV death and hospitalization for heart failure, both in DAPA-HF and EMPEROR-Reduced trials. So I think that's a critical point for clinicians to keep in mind at the time of the death. Dr Carolyn Lam: Mikhail, those are just such important and practical take-home messages. Thank you again. In the last minute though, I just really, really have to go back to that very clever method. Could I just pick your brain? I mean, it's like a very clever population. This CardioMEMS population that maybe what's in the future plans? Give us a sneak peek! Dr. Mikhail Kosiborod: Well, Carolyn, very insightful as always. I really think of it as a novel platform for drug development and heart failure. I think this is the proof of concept. This is really the first time we did something in the heart failure space was with monitoring of pulmonary pressures that shows that drugs that work for hard clinical outcomes actually do something meaningful on hemodynamics. We've struggled for such a long time in heart failure to have a good surrogate endpoints that would be reflective of clinical outcomes. This may be it. It may be one of them. And I think EMBRACE-HF is a good concept proving study that can say, if you have a compound and you think that compound may be effective for heart failure. So of course the congestion is so important that we know correlates so well with clinical outcomes Dr. Mikhail Kosiborod: When we started to trial all the way back to late 2015, very few patients had this device. It's not lots of patients have this device. And testing novel treatments to try to understand will there promise in heart failure, and even making go-no-go decisions, in terms of drug development, I think is starting to become a potential future development, which we should at least seriously consider in the heart failure space. Dr Carolyn Lam: Wow, Bravo. And Mikhail, I mean. Okay, audience, listen, you heard it right here. This is amazing. Thank you once again for publishing with us and congratulations on the beautiful paper. Dr Carolyn Lam: And from Greg and I, thank you audience for joining us again today, you've been listening to Circulation on the run. Tune in again next week. Dr. Greg Hundley: This program is copyright of the American Heart Association 2021.  

Interview with Jon S. Matsumura, and Sydney L. Olson, authors of Evaluating Growth Patterns of Abdominal Aortic Aneurysm Diameter With Serial Computed Tomography Surveillance

Interview with Jon S. Matsumura, and Sydney L. Olson, authors of Evaluating Growth Patterns of Abdominal Aortic Aneurysm Diameter With Serial Computed Tomography Surveillance

What does smoking have to do with Abdominal Aortic Aneurysms? Quite a lot, actually. Dr. Alain Bouchard and Dr. Adam Beck, an expert in vascular surgery at UAB, discuss all you ever needed to know about AAA.About the HostDr. Alain Bouchard is a clinical cardiologist at Cardiology Specialists of Birmingham, AL. He is a native of Quebec, Canada and trained in Internal Medicine at McGill University in Montreal. He continued as a Research Fellow at the Montreal Heart Institute. He did a clinical cardiology fellowship at the University of California in San Francisco. He joined the faculty at the University of Alabama Birmingham from 1986 to 1990. He worked at CardiologyPC and Baptist Medical Center at Princeton from 1990-2019. He is now part of the Cardiology Specialists of Birmingham at St. Vincent’s Health System, Ascension.Medical DisclaimerThe contents of the MyHeart.net podcast, including as textual content, graphical content, images, and any other content contained in the Podcast (“Content”) are purely for informational purposes. The Content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified health provider with any questions you may have regarding a medical condition. Never disregard professional medical advice or delay in seeking it because of something you have read or heard on the Podcast!If you think you may have a medical emergency, call your doctor or 911 immediately. MyHeart.net does not recommend or endorse any specific tests, physicians, products, procedures, opinions, or other information that may be mentioned on the Podcast. Reliance on any information provided by MyHeart.net, MyHeart.net employees, others appearing on the Podcast at the invitation of MyHeart.net, or other visitors to the Podcast is solely at your own risk.The Podcast and the Content are provided on an “as is” basis.

Take Home Points Consider ruptured AAA in patients (especially those > 50 years of age) with unexplained hypotension, back or abdominal pain All ruptured AAAs... The post REBEL Core Cast 49.0 – Abdominal Aortic Aneurysm (AAA) appeared first on REBEL EM - Emergency Medicine Blog.

THE DEATH OF EXPERTISE! In This Weeks Epsode Doc Morris Discusses the absurd new laws, putting all of Florida at serious health risk. Just wave a magic wand and make a nurse a physician. Can paralegals now practice law? How about the clerk selling light switches at Home Depot hiring on as a Journeyman electrician with FPL? Doc Morris Discusses These Dangerous New Laws This Week on Straight Talk with Doc Morris. Later in the Episode Doc Morris Discusses Geriatric Care. He Touches On Screening for Abdominal Aortic Aneurysm, Fracture Prevention in Older Adults, Exercise Prescriptions in Older Adults, Screening for Impaired Visual Acuity in Older Adults, Cancer Screening in Older Patients, and Screening for Hearing Loss in Older Adults. Below Are The News Laws Referenced By Doc Morris in This Episode:--- HB 607: Advanced practice registered nurses will have authority to practice independently of physicians, a top of priority of the legislative session for House Speaker Jose Oliva, R-Miami Lakes.--- HB 389: Pharmacists will be able to play an expanded role in providing health care to patients. In part, they will be able to enter “collaborative” agreements with physicians to treat patients for chronic illnesses, such as arthritis, asthma, chronic obstructive pulmonary diseases, Type 2 diabetes, HIV, AIDS and obesity. Rules still need to be finalized to carry out the bill.Find Out More about Doc Morris and his Practice at www.morrismedicalcenter.com or Email askdocmorris@morrismedicalcenter.com or Call 239-201-2465

In the May 2020 episode of the JAAPA Podcast, our co-hosts Kris Maday, PA-C and Adrian Banning, PA-C discuss CME articles on upper extremity compartment syndrome and on subclinical hypothyroidism. Then, they give a quick review of abdominal aortic aneurysm and discuss original research examining burnout and satisfaction with work life-integration in the PA profession. Plus, things get dramatic with cataclysmic events and cryptic messages from the past.

In this episode, we discuss the planning and treatment of Abdominal Aortic Aneurysms. We also focus on complications of open and endovascular repair with special attention to Endoleaks. 

I am Dr. Paul Kilgore, Host of the Quantitative Health Podcast. Please find me at quant@quantitative-health.com or my website: www.quantitative-health.com. Today, I discuss the very serious condition called Aortic Dissection and the companion condition, Abdominal Aortic Aneurysm. Aortic Dissection is believed to kill at least 13,000 Americans and many more around the world each year. Mr. Jamie Dimon, Chief Executive Officer of JP Morgan Chase and a well-known leader on Wall Street developed chest pain this past Thursday morning. Luckily, he got to the hospital a short time later and doctors found he had Aortic Dissection. Hear me today discuss this condition, how we diagnose, treat and prevent this condition and the Abdominal Aortic Aneurysm. Write me anytime with questions and please drop a quick rating of the podcast. I welcome your suggestions and comments to guide future episodes of the Quantitative Health Podcast. Thank you, Dr. Paul Kilgore, MD, MPH, FACP

I am Dr. Paul Kilgore, Host of the Quantitative Health Podcast. Please find me at quant@quantitative-health.com or my website: www.quantitative-health.com.  Today, I discuss the very serious condition called Aortic Dissection and the companion condition, Abdominal Aortic Aneurysm.  Aortic Dissection is believed to kill at least 13,000 Americans and many more around the world each year.  Mr. Jamie Dimon, Chief Executive Officer of JP Morgan Chase and a well-known leader on Wall Street developed chest pain this past Thursday morning. Luckily, he got to the hospital a short time later and doctors found he had Aortic Dissection. Hear me today discuss this condition, how we diagnose, treat and prevent this condition and the Abdominal Aortic Aneurysm.  Write me anytime with questions and please drop a quick rating of the podcast. I welcome your suggestions and comments to guide future episodes of the Quantitative Health Podcast.  Thank you, Dr. Paul Kilgore, MD, MPH, FACP

Listen as Dr. London Smith (.com) and his producer Cameron discuss Abdominal Aortic Aneurysm with special guest Sam Clemenson from the Extremely Offline Podcast. Not so boring! http://www.londonsmith.com/jockdocpodcast/30-abdominal-aortic-aneurysm-sam-clamenson/ Performed by: London Smith, Cameron Clark, Zaid Jilani, Dylan Walker. Written by: London Smith, Cameron Clark, Zaid Jilani, Dylan Walker. Produced by: London Smith, Cameron Clark, Zaid Jilani, Dylan Walker. Created by: London Smith  

Interview with Michael J. Barry, MD, USPSTF member and coauthor of Screening for Abdominal Aortic Aneurysm: US Preventive Services Task Force Recommendation Statement

Dr. Julie Freischlag is the dean of the Wake Forest University School of Medicine and the CEO of the Wake Forest University Baptist Medical Center. She did her general surgery training and vascular surgery fellowship at the University of California, Los Angeles where she later served as the Chief of the Section of Vascular Surgery. She went on to become the Chair of Surgery at Johns Hopkins University from 2003 - 2014. In 2013 she was elected as the first woman president of the Society for Vascular Surgery. She is the author of nearly 300 peer-reviewed journal articles and over 50 book chapters and has given over 250 invited lectures on a variety of topics in vascular surgery. Clinically, she has developed significant expertise in the management of thoracic outlet syndrome.  Throughout her career, she has demonstrated a notable dedication to teaching and mentoring the next generation of general and vascular surgeons. Thoracic Outlet Syndrome: A decade of excellent outcomes after surgical intervention in 538 patients with thoracic outlet syndrome. Orlando MS et al. J Am Coll Surg. 2015. The Art of Caring in Thoracic Outlet Syndrome. Editorial. Freischlag JA. Diagnostics. 2018, 8, 35. Remaining or Residual First Ribs are the Cause of Recurrent Thoracic Outlet Syndrome. Likes K et al. Annals of Vascular Surgery. 2014; 28: 939-945.  Video: Transaxillary First Rib Resection - Dr. Freischlag’s approach Aortic Aneurysm - The OVER trial: The Aneurysm Detection and Management Study Screening Program: Validation Cohort and Final Results. Lederle FA et al. Arch Intern Med. 2000;160(10):1425–1430.  Open versus Endovascular Repair of Abdominal Aortic Aneurysm. Lederle FA et al. NEJM. May 30, 2019. Leadership and Diversity in Healthcare: Developing Diverse Leaders at Academic Health Centers. A Prerequisite to Quality Health Care? Shaikh U et al. Am J of Medical Quality. 2018. If you enjoy our content, please contribute to Support Audible Bleeding! Tell us about yourself through our Fall 2019 Listener Survey!

Abdominal Aortic Aneurysms (AAA) can be life threatening. A AAA is when the part of the aorta that resides within the abdomen becomes bigger and bursts. Unfortuately, a AAA can develop slowly and not present with any symptoms. Occassionally people may feel a pulse near their belly button, or a pain in their back or stomach. Thankfully a thorough medical check up with a doctor can at times incidentally diagnose a AAA through investigations being conducted such as; vascular ultrasound imaging. Dr Peter Bray(Vascular Surgeon) today on MeditalkPodcast helps us better understand what is a AAA and how can a AAA be diagnosed and treated. If you are concerned about your health please make the time and speak with a medical pratitioner. Thank you for listening to MeditalkPodcast www.meditalk.com.au For more information about Dr Peter Bray please visit: www.sjog.org.au/find-a-doctor/search-results/b/r/a/y/bray-peter-subiaco If this podcast can help another person you know - please share. Please if you have a moment if you are able to rate or review Meditalk on Apple Podcasts would be a great help. Well wishes :-) D

On the Health and Fitness Show, Presenter Fahad Matin will be discussing 'Abdominal Aortic Aneurysm screening' with Dr Nadim Noor a Consultant Vascular Surgeon from the L&D.

Dr. Sara Honari explains what an endovascular aortic aneurysm is and how to repair it.

Rahul Sharma, DO discusses abdominal aortic aneurysm and how to treat this condition.

Kidney Stones are a Diagnosis of Exclusion!!! History Risk factors Age >60 Tobacco use Classic presentations Stable with sudden flank/back/abdominal pain or syncope Unstable with pallor, hypotension, and ill appearance Exam Pulsatile abdominal mass Unstable vitals Testing Plan Labs TYPE AND SCREEN CBC Electrolytes Coagulation studies Lactic acid Imaging Bedside ultrasound (optimal) Aorta protocol Look […]

Kidney stones are a diagnosis of exclusion. When you see flank pain or testicular pain or lower abdominal pain on that triage note, you have to consider leaking abdominal aortic aneurysm as well.

You place your hands on the patient's abdomen...you think you can feel it...thud...thud...thud... In the second part of our aortic syndromes series Dr Craig Douglas once again joined us to go through Abdominal Aortic Aneurysm (AAA) We discuss: - Definition of an aneurysm and pseudoaneurysm - The screening process for AAA - When to suspect AAA - Diagnosing and managing ruptured AAA - Craig and Jamie's mutual bugbear that a FAST scan does not look for the abdominal aorta! You can find the blog entry for this podcast including the #TakeVisually and a link to our #OHMNHS blog on the sensitivity and specificity of feeling an expansile-pulsatile mass at https://www.takeaurally.com/adult-emergency-medicine/2018/8/1/aortic-syndrome-part-two-abdominal-aortic-aneurysm Don't forget to subscribe to Take Aurally on SoundCloud and iTunes! NUH DREEAM and Take Aurally can both be found on Facebook and Twitter Next week's episode is on 'The Child with a Limp' - SUFE or not SUFE that is the question!

In this interview, Dr. Harminder Singh takes listeners through the new Canadian Task Force on Preventive Health Care (CTFPHC) guideline on screening for abdominal aortic aneurysm, or AAA. He explains each of the recommendations and the evidence behind them. Dr. Harminder Singh is associate professor of medicine in the departments of Internal Medicine and Community Health Sciences at the University of Manitoba. Dr. Singh is also a member of the CTFPHC and has co-authored the AAA guideline published in CMAJ.  Full guideline article (open access): www.cmaj.ca/lookup/doi/10.1503/cmaj.170118 ----------------------------------- Subscribe to CMAJ Podcasts on iTunes, Stitcher, Overcast, Instacast, or your favourite aggregator. You can also follow us directly on our SoundCloud page. Our podcasts are also released on www.cmaj.ca and on www.cmajblogs.com.

This episode covers Chapter 86 of Rosen’s Emergency Medicine. AAAs are our Great-White-Buffalo in emergency medicine. You need to know this!    List six presentations of an abdominal aortic aneurysm. Compare Aneurysm and Pseudoaneurysm List common misdiagnoses in patients with ruptured AAA List three common early and delayed complications of AAA repair List common delayed complications of Endovascular repair     Wisecracks:   What to do about the intact, asymptomatic aneurysm?    

This episode covers Chapter 86 of Rosen’s Emergency Medicine. AAAs are our Great-White-Buffalo in emergency medicine. You need to know this!    List six presentations of an abdominal aortic aneurysm. Compare Aneurysm and Pseudoaneurysm List common misdiagnoses in patients with ruptured AAA List three common early and delayed complications of AAA repair List common delayed complications of Endovascular repair     Wisecracks:   What to do about the intact, asymptomatic aneurysm?    

In this episode, we move on to the abdominal aortic aneurysms. Following this, we will talk about the most feared complication of aneurysms; dissection.

An Abdominal Aortic Aneurysm is a common and potentially deadly condition often seen in men over sixty. During today’s podcast, Dr. Dimitre talks about how to diagnose AAA’s and who should be screened in the family doctor’s office. Dr. Kevin shares with us his experiences with AAA and how its the white whale of many ER docs. […] The post Episode 28: Abdominal Aortic Aneurysm appeared first on Primary Medicine Podcast.

A complex abdominal aortic aneurysm is an abnormal ballooning of the wall of the aorta, the main artery supplying blood to the lower part of the body. This specific type of aneurysm is referred to as the “silent killer” since symptoms are often not present and if it ruptures, it often leads to death. Vascular surgeon, Dr. Wang Teng, discusses the causes and symptoms of a Complex Abdominal Aortic Aneurysm, as well as treatment using a fenestrated endovascular stent graft. Dr. Teng is one of few vascular surgeons in the nation trained to use the fenestrated endovascular stent graft, and was the first to perform the surgery in Southern California in January 2013.

As a bonus to Episode 26 on Low Back Pain Emergencies with Dr. Brian Steinhart & Dr. Walter Himmel, we have Dr. Walter Himmel's own personal incredible case of Cauda Equina Syndrome. In the related Episode we will cover the most serious spinal and vascular causes that present with low back pain including Cauda Equina Syndrome, Spinal Epidural Abscess, Spinal Epidural Hematoma, Metastases to the spine, Abdominal Aortic Aneurysm and Retroperitoneal Hematoma. [wpfilebase tag=file id=394 tpl=emc-play /] [wpfilebase tag=file id=395 tpl=emc-mp3 /] The post Best Case Ever 11: Cauda Equina Syndrome appeared first on Emergency Medicine Cases.

As a bonus to Episode 26 on Low Back Pain Emergencies with Dr. Brian Steinhart & Dr. Walter Himmel, we have Dr. Walter Himmel's own personal incredible case of Cauda Equina Syndrome. In the related Episode we will cover the most serious spinal and vascular causes that present with low back pain including Cauda Equina Syndrome, Spinal Epidural Abscess, Spinal Epidural Hematoma, Metastases to the spine, Abdominal Aortic Aneurysm and Retroperitoneal Hematoma. [wpfilebase tag=file id=394 tpl=emc-play /] [wpfilebase tag=file id=395 tpl=emc-mp3 /] The post Best Case Ever 11: Cauda Equina Syndrome appeared first on Emergency Medicine Cases.

In this episode, Aaron Banmann discusses the diagnosis and management of abdominal aortic aneurysm (AAA). After listening to this episode, learners will be able to: Define what an aneurysm is Describe how an aneurysm develops and list the risk factors for aneurysmal disease Describe how a patient with an AAA can present Outline how the diagnosis of AAA is made Describe the surgical treatment of an AAA Running time: 15:30  

Joan Stephenson, PhD, discusses Abdominal Aortic Aneurysm with Dr Frank Lederle.

JAMAevidence Podcast

Abdominal Aortic Aneurysm is often called a "silent killer" because there are usually no obvious symptoms of the disease. This talk focuses on the importance of knowing who is most at risk, how AAA is diagnosed and treated before it becomes fatal.